Our approach is to define in molecular terms the genetic complexity of the transformed state. While it is clear that many phenotypic differences exist between normal and transformed cells, it is no known whether this involves several host genes or a large number of host genes. The problem is further complicated by the fact that specific avian tumor viruses seem to have a rather well-defined host range for transformation that depends on the differentiated state of the infected cell. This raises the interesting question whether all cell types transformed by the same virus are, in fact, expressing the same genes and similarly, whether different viruses cause similar genes to be activated in the respective host cells they transform. We plan to deal with these questions by carrying out a detailed study of the nuclear and cytoplasmic RNA sequences characterizing the transformed state of a variety of cell types transformed by a number of different avian RNA tumor viruses. We hope (and our preliminary evidence supports this) that we can isolate a labeled DNA probe complementary to cellular RNA sequences specific for transformation. For convenience, we call such a probe cDNA(-ts) for complementary DNA-(tumor specific). Once isolated the probe will be used to study the structure of the template chromatin and the natural expression of these sequences during embryogenesis.